Anti-mannose binding lectin antibodies in sera of Japanese patients with systemic lupus erythematosus

R. Takahashi, A. Tsutsumi, K. Ohtani, D. Goto, I. Matsumoto, S. Ito, N. Wakamiya, T. Sumida

Research output: Contribution to journalArticlepeer-review

34 Citations (Scopus)


Mannose-binding lectin (MBL) is a key element in innate immunity with functions and structure similar to that of complement C1q. It has been reported that MBL deficiency is associated with occurrence of systemic lupus erythematosus (SLE). We hypothesized that anti-MBL antibodies, if present, would affect the occurrence or disease course of SLE, by reduction of serum MBL levels, interference of MBL functions, or binding to MBL deposited on various tissues. To address this hypothesis, we measured the concentration of anti-MBL antibodies in sera of 111 Japanese SLE patients and 113 healthy volunteers by enzyme immunoassay. The titres of anti-MBL antibodies in SLE patients were significantly higher than those in healthy controls. When the mean + 2 standard deviations of controls was set as the cut off point, individuals with titres of anti-MBL antibodies above this level were significantly more frequent in SLE patients (9 patients) than in controls (2 persons). One SLE patient had an extremely high titre of this antibody. No associations of titres of anti-MBL antibodies and (i) genotypes of MBL gene, (ii) concentrations of serum MBL, or (iii) disease characteristics of SLE, were apparent. Thus, we have confirmed that anti-MBL antibodies are indeed present in sera of some patients with SLE, but the significance of these autoantibodies in the pathogenesis of SLE remains unclear.

Original languageEnglish
Pages (from-to)585-590
Number of pages6
JournalClinical and Experimental Immunology
Issue number3
Publication statusPublished - Jun 2004
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology


Dive into the research topics of 'Anti-mannose binding lectin antibodies in sera of Japanese patients with systemic lupus erythematosus'. Together they form a unique fingerprint.

Cite this